• A master's degree (or equivalent) in life sciences, e.g. biology, biochemistry, medicine, veterinary medicine or pharmacy
• Hands-on experience in cell culture and molecular biology techniques
• Background knowledge in diabetes, pancreatic beta-cell biology, and/or incretin hormone-related signalling / metabolism is advantageous
• A strong interest in translational research with potential therapeutic implications
• An ambitious, innovative, and well-organized mindset, with the ability to work independently and as part of a collaborative research team
• Good communication skills and a solid command of English language

Visceral adiposity is a major risk factor for metabolic dysfunction and the development of type 2 diabetes (T2D). It promotes insulin resistance in adipose tissue, leading to an overflow of free fatty acids into the bloodstream. These fatty acids accumulate as ectopic fat in various organs, worsening the metabolic imbalance. The pancreas has emerged as a key site of ectopic fat deposition. While growing evidence suggests that pancreatic fat impairs beta-cell function and insulin secretion, its precise role in the pathophysiology of T2D remains unclear. To explore the crosstalk between pancreatic islets and adipocytes, we developed an innovative in vitro model of human primary pancreatic adipose organoids that retain donor-specific metabolic traits. Leveraging our “fatty pancreas-on-a-chip” platform, we aim to uncover cellular and molecular pathways through which adipocytes from distinct fat depots affect beta cell physiology and identify key mediators driving these inter-tissue interactions. Our overarching goal is to elucidate fat depot-specific mechanisms that impact islet function and drive diabetes pathogenesis, ultimately informing new therapeutic strategies for diabetes prevention and treatment.

For details about the RTG2816 please see: https://www.medizin.uni-tuebingen.de/de/medizinische-fakultaet/forschung/grks/rtg-2816